Emergency medicine

To the Editor: The benefits of bicycle helmet use have been the subject of recent discussion, with calls from some experts to review laws mandating the wearing of helmets.1 The objective of this brief report is to summarise long-term trends in cyclist head injuries seen at an inner-city major trauma centre and determine the odds of any skull fracture or intracranial bleed associated with not wearing a helmet. This was a retrospective study conducted at the Royal Prince Alfred Hospital (RPAH, Sydney, New South Wales), covering several local government areas that have the highest bicycle-use rates in NSW,2 where the law for mandatory helmet wearing was enacted in 1991. Patient data were obtained through the hospital trauma registry, which contains data on all patients admitted to the hospital with trauma. These data included information on helmet use routinely abstracted from ambulance and medical notes. Inclusion criteria were cyclists admitted from 1991 to 2009, who were over 16 years of age and involved in an incident on a public road. We excluded patients transferred from other hospitals. Head Abbreviated Injury Scale (AIS) scores (AIS 1990, 1998 and 2005 versions3) were used, with a head AIS score ≥ 3 indicating severe head injury, such as significant intracranial bleeding or depressed or comminuted skull fracture. Injuries with an AIS score of 2 included isolated concussion and simple skull fractures. To investigate the association between helmet use and head injury, we reviewed the medical charts of all cyclists admitted with trauma from 2008 to June 2010. We compared mechanism of injury (fall off bike without collision versus collision with another vehicle or object), anatomical injury (skull fracture or intracranial bleed), helmet use and the type of road where the incident occurred (state or regional roads versus local roads), according to NSW Roads and Traffic Authority classifications. Data were analysed using Stata software, version 10.1 (StataCorp, College Station, Tex, USA). Percentages were calculated with 95% confidence intervals, and categorical data were compared using χ2 tests. Mean ages were compared using the Student t test, and a logistic regression model was used to obtain odds ratios for any skull fracture or intracranial bleed associated with not using a helmet, after adjusting for mechanism of injury and road type. The study was approved by the Sydney South West Area Health Service RPAH Ethics Review Committee (RPAH Zone). There were 979 patients who met our inclusion criteria. The long-term trend in the number of cyclists sustaining severe head injuries remained low (range, 0–3 per year) (Box 1). Cyclists as a percentage of total admissions for trauma increased from 1.3% in 2005 (29/2258 [95% CI, 0.9%–1.8%]) to 3.9% in 2009 (122/3104 [95% CI, 3.3%–4.7%]). Trends in helmet use and severe head injury are summarised in Box 2. Severe head injury rates as a percentage of total cyclists admitted decreased from 10.3% (3/29 [95% CI, 3.6%–26.4%]) in 2005 to 2.5% (3/122 [95% CI, 0.8%–7.0%]) in 2009, a relative reduction of 76%. Helmet use in admitted cyclists from 1991 to 2009 ranged from 85% to 100%. Information was available about the location of the fall and helmet use for 287 of the 313 cyclists identified from 2008–2010 (Box 3). Their mean age was 36 years (95% CI, 34–37 years) and 81% were men. Non-helmet wearers had five times higher odds of intracranial bleeding or skull fracture compared with helmet wearers after adjusting for road type and mechanism of injury (odds ratio, 5.3 [95% CI, 1.7–17.1]; P = 0.005). The increase in admissions for bicycle injury is consistent with recently reported population trends.4 In addition, the number of cyclists sustaining severe head injuries has remained consistently low over the long term, with an apparent decline in the rate of severe head injuries in admitted patients since 2005. The odds reduction for skull fractures and intracranial bleeds in those wearing helmets is within the range reported in a Cochrane review of helmet use.5 The benefits of helmet use need to be placed in the context of lifetime costs of severe traumatic brain injury, estimated to be around $4.8 million per incident case.6 It is the opinion of the trauma service at RPAH, based on these findings, that mandatory bicycle helmet laws be maintained, and enforced as part of overall road safety strategies. 1 Trends in cyclist admissions and head injuries in admitted cyclists, RPAH, Sydney, New South Wales, 1991–2009 AIS = Abbreviated Injury Scale. RPAH = Royal Prince Alfred Hospital. 2 Trends in bicycle helmet use and severe head injury as a percentage of total cyclist trauma admissions, RPAH, Sydney, New South Wales, 1991–2009 AIS = Abbreviated Injury Scale. RPAH = Royal Prince Alfred Hospital. 3 Head injury in helmet and non-helmet users among 287 cyclists admitted to Royal Prince Alfred Hospital with trauma, 2008 to June 2010 Helmet (n = 241) No helmet (n = 46) Significance† Age, years (95% CI) 36 (34–38 years) 33 (29–37 years) P = 0.14 Men (%; 95% CI) 196 (81%; 76%–86%) 39 (85%; 71%–92%) P = 0.60 Fall off bicycle* (%; 95% CI) 83 (34%; 29%–41%) 13 (28%; 17%–43%) P = 0.75 State/regional road (%; 95% CI) 63 (26%; 21%–32%) 11 (24%; 14%–38%) P = 0.75 Skull fracture or intracranial bleed (%; 95% CI) 8 (3%; 2%–6%) 6 (13%; 6%–36%) P = 0.005 * Without direct collision with another vehicle, object or person. † Two-tailed P < 0.05 significant.

Michael M Dinh · Susan Roncal · Timothy C Green · Elizabeth Leonard · Amanda Stack · Chris Byrne · Jeffrey Petchell

To the Editor: It is incorrect for Chong and colleagues to state that “during the financial year 2006–07, 32 777 people were admitted to hospital in Australia due to road crashes”. It is also wrong for them to claim “it is often not clear how many of these road crashes are traffic crashes, and how many are non-traffic crashes”.1 Henley and Harrison report that there were 52 066 people seriously (but not fatally) injured due to land transport injury in 2006–07, and 32 777 of these (63.0%) occurred in traffic (on-road) accidents.2 A further 13 639 (26.2%) land transport injury cases in that year were explicitly described as non-traffic (off-road) accidents. The National Injury Surveillance Unit of the Australian Institute of Health and Welfare regularly publishes transport injury-specific analyses, including reports on land transport injuries (both traffic and non-traffic), rail-related transport injuries and transport injuries involving Indigenous Australians. The most recent of these reports is Henley and Harrison’s.2 In addition to the statistics mentioned above, they also report that the national age-standardised rate of non-traffic transport injuries was 66.5 per 100 000 population. In the previous year, this rate was 67.2 per 100 000 population.3 The next report in this series, to be published shortly, will include analysis of national trends in the rate of non-traffic transport injuries over the period 2000–01 to 2007–08.

Clare E Bradley · James E Harrison · Geoffrey I Henley

In reply: We acknowledge our error in reporting Henley and Harrison’s findings,1 and commend Bradley and colleagues for providing information about traffic and non-traffic transport injuries separately. We are also pleased that the National Injury Surveillance Unit will soon publish a report including analysis of trends in non-traffic transport injuries, extending our analyses beyond New South Wales. This is consistent with our conclusion that more needs to be done to understand non-traffic crashes.2 We defend our claim that the statistics in many reports and articles often do not clearly distinguish between traffic and non-traffic crashes and injuries.

Shanley S S Chong · Wei Du · Julie Hatfield

There is still room for improvement, both in decreasing delays in, and deciding who is eligible for, reperfusion therapy In patients with acute ST-segment-elevation myocardial infarction (STEMI), early coronary reperfusion — within 1 to 2 hours of symptom onset — by either thrombolysis or primary percutaneous coronary intervention (PCI) reduces the mortality rate by half. However, this benefit quickly dissipates with further delay in treatment.1 As “time is muscle”, it is the time from symptom onset to reperfusion (or total ischaemic time), rather than the mode of reperfusion, that is the critical determinant of outcome. Hence the imperative to minimise: (i) delay by patients in recognising symptoms as possible myocardial infarction (MI) and seeking medical help; (ii) delay in ambulances responding to calls; (iii) delays in diagnosing STEMI on first medical contact; and (iv) omissions or delays in administering the most appropriate means of reperfusion in eligible patients. In this issue of the Journal, Huynh and colleagues, using data from a prospective Australian registry, report on processes of care and outcomes of 755 patients presenting with suspected STEMI.2 There is good and bad news in this report. The good news is that the median time from symptom onset to first medical contact in this cohort was 105 minutes (1.75 hours) compared with 3.2 hours for patients with undifferentiated chest pain, reported in 2005.3 If the sample in the study by Huynh and colleagues2 is representative of most patients with MI, this suggests that public recognition of warning symptoms and the need to seek medical help urgently has improved over the past 15 years in response to public education campaigns that target individuals at high risk and behavioural barriers to action.4 Reperfusion reduced mortality at 12 months (adjusted for baseline risk as calculated using the Global Registry of Acute Coronary Events [GRACE] risk score) by 65% (and by 78% if administered in a timely fashion), similar to results noted in recent overseas observational studies that used similar risk-adjustment methods.5 Finally, there was no difference between metropolitan and rural patients in the time to presentation or the proportions of patients who received reperfusion therapy, or who received it in a timely manner, and the same applied to inhospital and 12-month mortality rates. This suggests the “city–bush” gap in coronary care noted in past studies6 is being closed, although more rural patients (74%) received thrombolysis, while more metropolitan patients (68%) received primary PCI. The bad news is that one in three patients did not receive any form of reperfusion — a figure common to other countries and which has proven resistant to change.7 Unfortunately, contraindications to either form of reperfusion in individual patients were not reported, but contraindications and patient refusal have been reported to account for no more than 10% of all patients with STEMI.8 This means just over one in five patients were likely to have been eligible for reperfusion therapy but failed to receive it. Factors associated with not receiving reperfusion therapy on regression analysis included a past history of diabetes or documented coronary stenoses on angiography, acute pulmonary oedema on presentation, left bundle branch block on electrocardiogram (ECG), and a non-cardiologist as the treating doctor. In other studies of patients eligible for reperfusion therapy, additional factors have included older age, admission to a facility not capable of performing PCI, increasing time to presentation, renal insufficiency, prior stroke or coronary artery bypass grafting, being female, and presentation without chest pain or with an equivocal ECG.5,7 Some of these associations reflect diagnostic uncertainty in patients with atypical clinical presentations and non-diagnostic ECGs or clinician concern about the risk of bleeding in older patients (especially underweight women) and those with renal failure or prior stroke. However, registry data show that in this patient group at relatively high risk, early reperfusion therapy compared with no reperfusion reduces inhospital mortality by 38%, with primary PCI being more effective than thrombolysis.9 Clinicians may need to recalibrate their perceptions of benefit and risk in groups of patients who have often been excluded from clinical trials. The other bad news is that among patients receiving reperfusion therapy in the study by Huynh and colleagues (61%, primary PCI; 37%, thrombolysis), only one in three received it within an optimal time frame.2 The median door-to-needle time (D2N) for thrombolysis was 43 minutes (versus a 30-minute standard) and door-to-balloon time (D2B) for primary PCI was 102 minutes (versus a 90-minute standard). These times are longer than those reported in contemporary cohorts in other developed countries, such as 33 minutes D2N and 83 minutes D2B in a Canadian cohort,5 and 30 minutes D2N and 86 minutes D2B in the GRACE international registry.10 Attention has recently shifted to reducing total system delay, defined as the time from first contact with the health care system (ie, ambulance) to initiation of reperfusion therapy, which now appears to be more strongly associated with mortality than patient delay in seeking care.11 In reducing system delay, the timing of PCI (immediate v delayed v rescue) and its relation to thrombolysis in patients presenting to non-PCI-capable hospitals becomes a pivotal issue. Current Australian and New Zealand guidelines state that fibrinolysis is preferred to primary PCI in patients presenting within 1 hour of symptom onset unless balloon insufflation can occur within 60 minutes after first medical contact (in most cases, this is patient pick-up by ambulance).12 In patients presenting between 1 and 3 hours after symptom onset, fibrinolysis is preferred unless primary PCI can occur within 90 minutes of first medical contact. Studies show that in patients with symptom onset of less than 3 hours and for whom transfer to PCI-capable hospitals would delay primary PCI for more than 90 minutes, the combination of early lysis and aggressive use of rescue PCI (in the third of patients with persistent ST-segment elevation, cardiogenic shock, severe heart failure or serious ventricular arrhythmias) confers comparable outcomes with that achieved with primary PCI.13 In this regard, prehospital thrombolysis undertaken by ambulance paramedics, combined with early PCI where appropriate, seems to be an underused strategy in reducing system delay.14 Another issue is the role of risk stratification in deciding who should receive which form of reperfusion. A treatment-risk paradox is often seen whereby eligible patients at high absolute risk of death or recurrent MI are less likely to receive reperfusion therapy (for reasons already mentioned) than those at lower risk9 and in whom treatment delays attenuate the absolute benefit of reperfusion to a greater degree. In considering transferring patients presenting within 6 hours of symptom onset for primary PCI, the higher the risk profile, the larger the reduction in mortality benefit with primary PCI compared with thrombolysis for each 10-minute increase in PCI-related time delay.15 Delays must be minimised in high-risk patients, rather than simply working to a 60-minute or 90-minute D2B rule. The equipoint between primary PCI and fibrinolysis (the PCI-related time delay at which primary PCI loses its superiority in terms of mortality benefit compared with fibrinolysis) may be as little as a D2B time of 40 minutes in a high-risk situation (such as a young patient presenting early with a large anterior infarction) versus 179 minutes in lower risk situations (such as an older patient presenting late with a non-anterior infarction).16 Several strategies have been shown in both Australian and overseas studies to be effective in reducing total ischaemic time (Box),17-19 and these need to become mainstream care. This will require a multifaceted approach involving educating both patients and doctors; coordinating ambulance, emergency department and cardiac catheterisation laboratory components of care; establishing integrated networks of non-PCI and PCI-capable hospitals with decision support and transfer processes that take patient risk and time to presentation into account; and ongoing data collection and feedback within clinical registries. Strategies for decreasing delays in reperfusion therapy Hospital-based strategy Potential tools Prehospital ECG and field assessment by paramedics Prehospital ECG policy Guidelines for field assessment with electronic transmission to, and verification of ECG diagnosis by, emergency department staff Prehospital thrombolysis for patients who are within 1 hour of symptom onset Training of paramedics in ECG diagnosis and administration of thrombolytic agents Transfer of PCI-eligible patients direct to a PCI-capable facility Pre-destination protocol for paramedics Rapid assessment and ECG on patients presenting to emergency departments with chest pain Dedicated chest pain cubicles in emergency departments with ECGs taken within 10 minutes of arrival Rapid management of diagnostically uncertain cases Formal order sets for suspected myocardial infarction in cases of initially non-diagnostic ECG Rapid initiation of thrombolysis in eligible patients Formal thrombolysis protocols that can be initiated by emergency department nurses or physicians without consulting the cardiology department Emergency department bypass of PCI-eligible patients with direct transfer to a catheterisation laboratory Prehospital (or first hospital) assessment policy Guidelines for direct activation of the catheterisation laboratory by emergency department staff without review or approval by cardiologists Single-call activation of the catheterisation laboratory team Alert system with single person as contact (senior registrar or consultant) Catheterisation team fully operational within 30 minutes of activation Staff policy and roster Performance of PCI 7 days a week, 24 hours per day Clearance of elective cases; maintained availability of ready-to-go equipment and staff Prompt data feedback Time-entry forms for door-to-needle and door-to-balloon times, and these times notified to all team members after each procedure Team-based approach Team training program; limited handovers with single team approach Regionalised “hub-and-spoke” hospital networks which expedite patient transfer to PCI-capable facility Triage and expedited transfer guidelines for referring and receiving hospitals PCI = percutaneous coronary intervention. ECG=electrocardiogram.

Ian A Scott FRACP, MHA, MEd

Providing world-class stroke care in Australia Cerebrovascular disease is the third leading cause of disease burden in developed nations, and is predicted to be the fourth ranked disease burden worldwide by 2030 after unipolar depressive disorders, ischaemic heart disease and trauma.1 All of these conditions are characterised by sudden and unpredictable demands requiring an immediately accessible, systemised and multidisciplinary approach to care. The complexities of acute ischaemic stroke in Australia have been addressed by detailed clinical guidelines.2 An emergency care bundle for stroke and transient ischaemic attack has recently been offered by the National Institute of Clinical Studies of the National Health and Medical Research Council.3 When administered to appropriate patients within 3 hours of stroke symptom onset, the benefits of recombinant tissue plasminogen activator (rt-PA) are significant, with treated patients 30% more likely to be in the excellent outcome grade — an absolute increase of 13%4 — and improvements in modified Rankin scores for some other patients with higher modified Rankin scores. The number of patients needed to treat for benefit may be as low as three.5 The associated risk of an intracerebral haematoma causing deterioration is about one in 30.5 The third European Cooperative Acute Stroke Study (ECASS3), a randomised trial of intravenous rt-PA in the 3–4.5 hour window, demonstrated a smaller but statistically significant benefit with no increase in haematoma rate.6 A recent Cochrane review of 26 thrombolysis trials of rt-PA, streptokinase, desmoteplase, urokinase and pro-urokinase, which included 7125 patients, found a significant net benefit in terms of death and dependency.7 The clinical applicability of new therapies may be exaggerated by the Hawthorne effect of clinical trials. The European Safe Implementation of Thrombolysis in Stroke Monitoring Study (SITS-MOST) registry — a mandated requirement of European drug licensing authorities — was established to monitor thrombolysis in day-to-day clinical practice.8 It included centres not experienced with thrombolysis and demonstrated the feasibility and safety of thrombolytic therapy across Europe. The cover of the issue of The Lancet in which the registry outcomes were published declared that rt-PA is “safe and effective in routine clinical use”. The rate of symptomatic intracerebral haemorrhage (ICH), as defined by the National Institute of Neurological Disorders and Stroke (NINDS), was 7.3% in SITS-MOST for both experienced and new thrombolysis centres, with a calculated mortality rate from ICH at 3 months of 1.9%.8 Early deterioration due to ICH in the SITS-MOST registry occurred in 1.7% of cases. In this issue of the Journal, Simpson and colleagues report the Australian contribution to the Safe Implementation of Thrombolysis in Stroke International Stroke Thrombolysis Register (SITS-ISTR),9 reflecting the local experience of treating acute stroke 15 years on from the NINDS trial.4 Participation in the Australian component of the SITS-ISTR was voluntary. Many centres undertaking thrombolysis did not participate, and this may weaken the generalisability of this new data. Nevertheless, over 500 patients were enrolled and outcomes did not differ from those of the larger international database. The important safety data were reassuring, with a symptomatic ICH rate of 8.3% by the definition used in the NINDS randomised controlled trial, and 1.3% by the SITS-MOST definition. The 3-month ICH mortality rate was 2.2%. A British subset of SITS has been reported recently, with outcomes also comparable to those for the rest of Europe.10 In the SITS-MOST registry, new and experienced centres did not differ in terms of their haemorrhagic complication rates.8 While the Australian report by Simpson et al does not detail information regarding the types of centres involved, implementation of thrombolysis in Australia beyond the centres that participated in the thrombolysis trials is already well established. Audits by the National Stroke Foundation have found that 33 hospitals were regularly treating with rt-PA in 2007,11 and that this increased to 50 by 2009.12 New metropolitan and rural centres can adopt thrombolysis with executive support and leadership from medical and nursing “stroke champions”. This nearly always results in the establishment of a stroke unit and the adoption of a local thrombolysis protocol with coordination of the prehospital emergency services. Mentorships with established metropolitan centres are worthwhile in the early stages. Some direct links using telemedicine for the treatment of the first cases have been employed in Victoria (Associate Professor Bernard Yan, Neurologist and Neurointerventionist, Royal Melbourne Hospital, personal communication). Early recognition and intervention for stroke requires a tightly coordinated interdisciplinary approach and rates of intravenous thrombolysis administration can be used as a clinical quality indicator for stroke care.13 Ongoing participation in the SITS-ISTR and the Australian Stroke Clinical Registry is crucial for monitoring the progress of this important therapy. A coordinated system of care for stroke and transient ischaemic attack in Australia has been stalled by the lack of a concerted effort to adopt thrombolysis. Australian registry data provide reassurance that Australian stroke physicians, emergency physicians and systems that support thrombolysis can achieve similar results to those recorded in Europe. We can now move beyond discussing the efficacy and feasibility of implementing this therapy and work toward a more coordinated system of applying the evidence.

Mark Fitzgerald MB BS, FACEM · Richard P Gerraty MD, FRACP

Aim: Design, setting and participants: Retrospective observational study of patients who were tested for influenza A after being admitted to hospital through emergency departments of the Sydney South West Area Health Service from 15 June to 30 August 2009.Main outcome measures: The association of factors such as age, diagnosis at admission, hospital and week of admission with rates of testing and detection of influenza A.Results: 17 681 patients were admitted through nine emergency departments; 1344 (7.6%) were tested for influenza A, of whom 356 (26.5%) tested positive for pandemic influenza. Testing rates were highest in 0–4-year-old children, in the peak period of the outbreak, and in patients presenting with a febrile or respiratory illness. Positive influenza test results were common across a range of diagnoses, but occurred most frequently in children aged 10–14 years (64.3%) and in patients with a diagnosis at admission of influenza-like illness (59.1%). Using multivariate logistic regression, patients with a diagnosis at admission of fever or a respiratory illness at admission were most likely to be tested (odds ratios [ORs], 15 [95% CI, 11–21] and 17 [95% CI, 15–19], respectively). These diagnoses were stronger predictors of influenza testing than the peak testing week (Week 4; OR, 7.0 [95% CI, 3.8–13]) or any age group. However, diagnosis at admission and age were significant but weak predictors of a positive test result, and the strongest predictor of a positive test result was the peak epidemic week (Week 3; OR, 120 [95% CI, 27–490]).Conclusion: The strongest predictor of a clinician’s decision to test for influenza was the diagnosis at admission, but the strongest predictor of a positive test was the week of admission. A rational approach to influenza testing for patients who are admitted to hospital for acute care could include active tracking of influenza testing and detection rates, testing patients with a strong indication for antiviral treatment, and admitting only those who test negative to “clean” wards during the peak of an outbreak.

Andrew Jardine PhD, MAE · Stephen J Conaty MB BS, MPH, FAFPHM · Michelle A Cretikos MPH, PhD, FAFPHM · Wei-Yuen Su MB BS · Iain B Gosbell MD, FRACP, FRCPA · Sebastiaan J van Hal MB ChB, FRACP, FRCPA

Introducing an innovative, evidence-based resource for use in the emergency department In early 2008, the National Institute of Clinical Studies (NICS) Stroke Clinical Reference Group was formed to develop an acute stroke care resource for use in emergency departments (EDs) in Australian hospitals. The NICS reference group used a care bundle approach to develop a guideline implementation tool based on specific recommendations from the 2007 National Stroke Foundation (NSF) Clinical guidelines for acute stroke management relevant for ED care.1 Although these guidelines were already available, there are well known barriers to guideline implementation in the ED. These include increasing demand and acuity, and the broad diversity of clinical presentations. Clinical information provided for ED clinicians needs to be concise and relevant to the emergency care context. The nine-member NICS reference group represented a collaboration between stroke and ED specialists, prehospital providers and managers of state-based stroke networks, with additional guidance from the NSF. Over the following 12 months, a consultative process took place, with a combination of face-to-face and teleconference meetings and email exchanges. The reference group used a Delphi process to reach consensus. In December 2009, the NICS released two documents — the Emergency department stroke and TIA care bundle: information and implementation package and the accompanying Summary for clinicians. These are available on the National Health and Medical Research Council (NHMRC) website (http://www.nhmrc.gov.au/nics/programs/emergency/stroke_tia.htm). This editorial presents a précis of the care bundle. Care bundles have already been shown to improve guideline compliance and lead to improved patient outcomes in several settings, including the ED.2-6 A care bundle is made up of a small number of best-practice recommendation components, is not as comprehensive as a guideline, and aims to identify critical recommendations relating to areas in which there is a significant practice gap or to act as a trigger to other best practice.7 The NICS care bundle needed to bring together several components to help clinicians provide quality care to adult patients who present to the ED with suspected stroke or transient ischaemic attack (TIA) by reducing morbidity and mortality and optimising patient outcomes (Box 1). The criteria for a component’s inclusion in the care bundle were determined by the model developed by the Institute for Healthcare Improvement in the United States:7 each component must be based on sound evidence; the delivery of each component must need improvement; the delivery of each component must be achievable in terms of universally available resources; no component should be a major source of controversy; and the delivery of each component must be measurable. Two components — stroke unit care and thrombolysis — are not included in the care bundle. We acknowledge the importance of stroke unit care — and thrombolysis for patients who meet the criteria for its use — when appropriate resources are available. The NSF recommendations, along with similar international guidelines, state that thrombolysis should only be given under the authority of a specialist team with expert knowledge of stroke management and with pathways and protocols in place to guide the acute phase.1,8-10 Although there is level I evidence that thrombolysis and stroke unit care are effective early interventions for stroke,2 currently thrombolysis is only offered in 28% of acute hospitals that manage stroke patients, and stroke unit care is only available in a third of hospitals across Australia.8 The reference group considered all of these factors and decided, by consensus, not to include thrombolysis and stroke unit care in the care bundle, as the necessary resources to support these are not universally available. However, the reference group believes that an emphasis on the first component of the bundle — a rapid initial stroke screen — could lead to earlier referral to stroke specialists and rapid access to computed tomography or magnetic resonance imaging to confirm the diagnosis and develop a management plan that would consider thrombolysis if clinically appropriate.11 This illustrates how the components of the care bundle may trigger additional best-practice recommendations as a natural consequence and establish joint clinical decision making with other disciplines to improve patient care (Box 2). The NICS clinical reference group is planning to collaborate with key stakeholders in 2010 to evaluate the effectiveness of the care bundle, both as a format for providing specific guideline recommendations to a target audience and in terms of the impact on stroke care in the ED. An implementation plan and auditing tool have also been developed to assist in the uptake of the recommendations. The NICS care bundle is based on the 2007 NSF clinical guidelines,1 and its recommendations are consistent with the current draft of the 2010 NSF guidelines. It is intended that the care bundle will evolve to ensure that recommendations relevant to the ED remain current. 1 Components of the NICS care bundle Rapid initial stroke screen (grade C; level II)* ABCD2 assessment† for suspected TIA (grade B; level II) Urgent‡ CT or MRI (grade A; level I) Nil by mouth until bedside swallow screen (within 24 hours) for stroke (grade C; level I) Aspirin as soon as possible,§ if haemorrhage excluded (grade A; level I): 150–300 mg one-time loading unless contraindicated Physiological monitoring and treatment Neurological status (grade C; levels II and III-2): regular monitoring to establish baseline and identify change Blood glucose (grade B; level II): cautious treatment of markedly elevated blood glucose levels; early, intensive maintenance of euglycaemia is not recommended. Avoid hypoglycaemia Blood pressure (consensus¶): cautious lowering by no more than 10%–20% if extremely high (≥ 220/120 mmHg); monitor for neurological deterioration Hydration status (grade B; level II): maintain euvolemia NICS = National Institute of Clinical Studies. TIA = transient ischaemic attack. CT = computed tomography. MRI = magnetic resonance imaging. * Evidence-based grades and levels as per 2007 National Stroke Foundation clinical guidelines.1 † A seven-point score calculated from age, blood pressure, clinical features, duration of symptoms, and diabetes status. ‡ “Urgent” means as soon as possible, but certainly within 24 hours.1 § “As soon as possible” means within 48 hours.1 ¶ Recommended best practice based on clinical experience and expert opinion. 2 Application of the NICS care bundle* Case study 1: a 68-year-old man presents to a hospital emergency department (ED), having woken with marked weakness of his left arm. Enquiry establishes that he was fine when he went to bed 7 hours earlier. The patient’s blood pressure (BP) at triage is 186/99 mmHg. The triage nurse is concerned that the patient is having a stroke. Case study 2: a 74-year-old woman with a history of type 2 diabetes mellitus and hypertension presents to a metropolitan tertiary hospital ED. She is unable to speak and has no strength in her right arm or right leg. Her friend states that the symptoms started only 2 hours ago. The patient’s BP is 170/95 mmHg; her heart rate is 80 beats/min and the heart is in sinus rhythm; and her blood glucose level is 9 mmol/L. The following care is provided for these patients, consistent with the use of the care bundle: as part of the patient’s assessment, and based on clinical findings, conduct a rapid initial stroke screen using a validated stroke screening tool to determine whether the patient is likely to have had a stroke. If a stroke is suspected, promptly refer the patient for expert stroke management — this may include referral to a stroke unit, or thrombolytic treatment (which is likely for the patient in case study 2); order an urgent computed tomography (CT) scan of the brain; ensure no oral intake until the patient undergoes a swallow screen for dysphagia; maintain hydration via intravenous or nasogastric fluids; administer aspirin (150 mg) within 48 hours if the brain CT scan excludes haemorrhage (if the patient in case study 2 proceeds to thrombolysis, delay aspirin treatment until 24 hours after thrombolysis); monitor the patient’s neurological status, blood glucose level, BP and hydration status to prevent further deterioration. NICS = National Institute of Clinical Studies. * The NICS care bundle was written for the care of stroke patients while in the ED. If the patient is transferred out of the ED early in his or her care, it is anticipated that the remaining components of the bundle will still be provided in the new setting.

Jayantha I Weeraratne MB BS, FACEM · Annette J Lenstra BSc, GradDip(Gov) · Andrew W Lee MB BS, MPH, FRACP · Kelvin M Hill BAppSci(Physio), GradDip(BusComm) · Susan D Huckson BAppSci, RN, ICU(Cert) · Jodie L Clydesdale BNurs, GradDip(ClinNurs)

To the Editor: The Between the Flags project of the Clinical Excellence Commission (CEC) is designed to establish a “safety net” in all New South Wales public hospitals, to enable early identification and management of deteriorating hospital inpatients.1 A paediatric advisory group within of the program is currently developing five age-group-specific paediatric observation charts to account for the changes in normal physiological parameters that occur with age in children, and these have been distributed for comment before finalisation. Each chart has specific physiological calling criteria defining when a clinical review or rapid response is required from medical staff (Box). If one or more criteria fall in the “red” zone, the patient requires an immediate, rapid response; if criteria fall in the “yellow” zone, the patient needs a clinical review within 30 minutes. A paucity of data on what represents an abnormal parameter for each age group has also led to a lack of clear triage guidelines for emergency department nurses. For example, the paediatric physiological discriminators of the Australasian Triage Scale include terms such as “mild tachycardia” as a guide for allocating patients to triage Category 3 and “moderate tachycardia” for Category 2.2 We trialled the CEC paediatric inpatient calling criteria to determine whether they could also be used for emergency department triage purposes. We carried out a retrospective review of patients presenting to triage at the emergency department of the Children’s Hospital at Westmead between 1 and 14 March 2010. We assumed that patients who met the CEC’s yellow criteria should be allocated to triage Category 3 (“urgent: review within 30 minutes”) and those who met the CEC’s red criteria should be allocated to at least triage Category 2 (“emergency: review within 10 minutes”). Patient outcomes were classified as “admitted”, “discharged” or “did not wait”. From 1968 presentations, 1885 patients had observations at triage available for review. The numbers of patients in each triage category were: Category 1 (5); 2 (41); 3 (403); 4 (422); and 5 (1014). Only 10 of the 46 patients in Category 1 and 2 would have been flagged by the CEC parameters as needing a rapid response (ie, review within 10 minutes), and none of the three patients admitted to the paediatric intensive care unit would have been identified by the CEC parameters. Of the 403 patients in Category 3 (needing review within 30 minutes), 32 would have been uptriaged to Category 2 by the CEC criteria. Twelve of these 32 patients were in fact discharged home, indicating that the CEC criteria are unsuitable for triage purposes. Of the 1436 patients in Category 4 and 5, 30 would have been uptriaged to Category 2 according to the CEC parameters and, of these, only three were admitted. A further 271 patients would have been uptriaged to Category 3 (181 of these were discharged and 54 did not wait). Of particular note is that 151 of the 271 patients met the yellow criteria because of low respiratory rates that were flagged by the charts but were normal for the patient. At present, the physiological parameters defined in the new CEC paediatric inpatient observation charts are not suitable as a triage tool in the paediatric emergency department, do not replace an experienced triage nurse, and are a poor predictor of disposition. CEC calling criteria* and physiological parameters for children, by age group Calling criteria, by age group Call Physiological parameter < 30 days 1–12 months 1–4 years 5–11 years ≥ 12 years Red† Heart rate (beats/min) Above 180 190 170 160 150 Below 80 80 70 60 40 Respiratory rate (breaths/min) Above 100 65 60 50 40 Below 20 15 15 10 5 Systolic blood pressure (mmHg) Above — — — — — Below 60 50 70 70 80 Oxygen saturation (%) Below 85 85 85 85 85 Temperature (°C) Above 38 — — — — Yellow‡ Heart rate (beats/min) Above 160 170 150 140 130 Below 90 100 80 70 50 Respiratory rate (breaths/min) Above 60 50 50 35 30 Below — 30 20 15 10 Systolic blood pressure (mmHg) Above — 120 120 130 160 Below 70 80 80 80 90 Oxygen saturation (%) Below 95 90 90 90 90 Temperature (°C) Above 37.5 — — — — CEC = Clinical Excellence Commission. * Calling criteria as of March 2010 at the time of this study (the CEC has subsequently revised some of these criteria). Only one “flag” was required to meet a calling criterion. Other calling criteria such as pain, work of breathing and level of consciousness were not measured in our study but will also generate a call. Where no values are present, there are no calling criteria for the parameter. † Red call requires immediate, rapid response. ‡ Yellow call requires review within 30 minutes.

Fenton M O’Leary · Jennifer I Major

Objectives: To determine which laboratory tests are first associated with severe envenoming after a snakebite, when (ie, how long after the bite) the test results become abnormal, and whether this can determine a safe observation period after suspected snakebite.Design, patients and setting: Prospective cohort study of 478 patients with suspected or confirmed snakebite recruited to the Australian Snakebite Project from January 2002 to April 2009, who had at least three sets of laboratory test results and at least 12 hours of observation in hospital after the bite. Severe envenoming was defined as venom-induced consumption coagulopathy (VICC), myotoxicity, neurotoxicity or thrombotic microangiopathy.Main outcome measures: International normalised ratio (INR), activated partial thromboplastin time (aPTT), creatine kinase (CK) level, and neurological examination.Results: There were 240 patients with severe envenoming, 75 with minor envenoming and 163 non-envenomed patients. Of 206 patients with VICC, 178 had an INR > 1.2 (abnormal) on admission, and the remaining 28 had an INR > 1.2 within 12 hours of the bite. Of 33 patients with myotoxicity, a combination of CK > 250 U/L and an abnormal aPTT identified all but two cases by 12 hours; one of these two was identified within 12 hours by leukocytosis. Nine cases of isolated neurotoxicity had a median time of onset after the bite of 4 hours (range, 35 min – 12 h). The combination of serial INR, aPTT and CK tests and repeated neurological examination identified 213 of 222 severe envenoming cases (96%) by 6 hours and 238 of 240 (99%) by 12 hours.Conclusion: Laboratory parameters (INR, aPTT and CK) and neurological reassessments identified nearly all severe envenoming cases within 12 hours of the bite, even in this conservative analysis that assumed normal test results if the test was not done.

Graham Ireland MB BS · Simon G A Brown FACEM, PhD · Nicholas A Buckley BMed, FRACP, MD · Jeff Stormer RN · Bart J Currie MB BS, FRACP · Julian White MB BS, MD · David Spain MB BS, FACEM · Geoffrey K Isbister BSc, FACEM, MD

Objectives: To describe the characteristics, management and outcomes of patients with major trauma who were taking warfarin; explore the use of rapid anticoagulation reversal; and assess the effect of reversal on outcomes.Design and setting: Retrospective cohort analysis of prospective data extracted from the trauma registries and patient charts of the two adult trauma referral hospitals with neurosurgical units in Western Australia, 2000 to 2005. Inclusion criteria were: major trauma (injury severity score > 15); first international normalised ratio (INR) after injury > 1.4; and documented (in registry or chart) warfarin use.Results: Eighty patients were identified. Their mean age was 76.8 years. Forty-six were men; 34 were transferred from another hospital; 28 died; and the functional outcomes of 58 were worse at discharge from hospital than before injury. Intracranial haemorrhage (ICH) occurred in 62, of whom 25 died; the difference in mortality between those with ICH and those without ICH was insignificant. Warfarin reversal started 17.4 hours (mean) after injury and the documented period between injury and completion of reversal was 54.2 hours (mean). Multiple logistic regression models, controlling for age, sex, on-scene Glasgow Coma Scale (GCS), initial INR and progressive ICH, showed no independent survival benefit for rapid reversal. Factors associated with mortality were age (22% increase per year [95% CI, 17%–34%]) and progressive ICH on computed tomography scan (24 of the 36 patients with progressive ICH died v one of the 26 patients with stable ICH died). Every point increase in on-scene GCS > 8 increased survival likelihood by 215% (95% CI, 119%–388%).Conclusions: Patients with major trauma taking warfarin at the time of injury have high mortality rates, poor functional outcomes and long delays to initiation and completion of anticoagulation reversal. Rapid, appropriate warfarin reversal was rarely performed and was not independently associated with survival. Age, low on-scene GCS and progressive ICH were strongly associated with mortality, but presenting INR, ICH v no ICH, and sex were not.

David Mountain MB BS, FACEM · Vera Sistenich MB BS, FACEM · Ian G Jacobs BAppSc, PhD, RN

Objectives: To assess whether a collaborative interdepartmental pathway involving emergency department (ED) physicians activating the cardiac catheterisation laboratory (CCL) with immediate patient transfer to the CCL reduces door-to-balloon (DTB) times for patients with suspected ST-elevation myocardial infarction (STEMI).Design, setting and participants: A quasi-experimental before-and-after observational study using a prospective database, supplemented by chart review, of consecutive patients transferred from the ED to the CCL for suspected STEMI, from January 2007 to October 2009, at Sir Charles Gairdner Hospital, an adult tertiary-care hospital, Western Australia.Main outcomes measures: Median DTB time and proportion of patients with DTB time of < 90 minutes. Secondary outcomes, based on analysis of predefined subgroups, included door-to-activation time, activation-to-balloon time and false-positive activations of the CCL.Results: Two hundred and thirty-four patients underwent emergency coronary angiography for suspected STEMI, with 188 (80%) undergoing percutaneous coronary intervention (118 before and 70 after implementation of the new pathway). Following implementation of the new pathway, median DTB time reduced from 97 to 77 minutes (P < 0.001), median door-to-activation time from 28 to 15 minutes (P = 0.002) and median activation-to-balloon time from 66 to 53 minutes (P < 0.001). The proportion of patients with recommended DTB time of < 90 minutes increased from 41% to 77% (P < 0.001) with no change in false positive CCL activation rates (12% v 11%; P = 0.38).Conclusion: ED physician activation of CCL with immediate patient transfer is associated with highly significant improvements in DTB time without increased false positive rates.

Alexander B Willson MB BS(Hons), MPH, FRACP · David Mountain MB BS, FACEM · Joanne M Jeffers MB BS · Cheryl G Blanton MSc · Brendan M McQuillan MB BS, PhD, FRACP · Joseph Hung MB BS, FRACP, FCSANZ · Michael H Muhlmann MB BS, FRACP · Michael C Nguyen MB BS, FRACP

Increasing numbers of patients are presenting for unscheduled medical admission to hospitals worldwide, prompting clinical redesign of “front-door” emergency medical services. In the United Kingdom, there has been considerable investment in the establishment of acute medical units (AMUs) and the training of acute medicine physicians. Some centres in Australia have established similar medical assessment units. While these initiatives have undoubtedly met with some success, the evidence base for their overall benefit remains elusive. We describe key aspects of the recent establishment of acute medical services in Britain and discuss the relevance of these experiences to Australia. Successful models of care in acute medicine have often been shared with other centres. The adaptation of existing models of care to meet local demands is superior to simply adopting an existing model. Once the desired clinical functionality of a service is determined, informed decisions can be made on staffing requirements, skill mix, and the structure of any new clinical unit. The functionality of the acute medical service, rather than simply the physicality of an AMU, should drive service design.

Paul F Jenkins MA, MB, FRCP · Lorna L Barton MB BS, MRCP · Gregor B S McNeill MB ChB, MRCP

Prompt myocardial reperfusion, particularly if achieved within 2 hours of the onset of symptoms, improves outcomes in patients with ST-elevation myocardial infarction (STEMI). Recent data suggest that ambulance-administered prehospital thrombolysis, if given within 2 hours of the onset of STEMI, produces superior outcomes to primary percutaneous coronary intervention (PCI); if given within 4 hours, the outcomes are similar. For optimal results after thrombolysis, patients require angiography (and PCI where appropriate) within 24 hours of the event. These developments have major implications for the practice of cardiology and for the organisation of health services in Australia.

Richard W Harper MB BS, FRACP, FACC · Jeffrey Lefkovits MB BS, FRACP, FCSANZ

To the Editor: Many of the arguments put forward by Bain and colleagues about modelling hospital occupancy1 are true in an academic sense. We agree that many acute care models use simplified inputs and outputs, without accounting for rapid daily fluctuations in occupancy. Occupancy definitions are often misleading and subject to gaming. We agree with the work by Bain, Taylor and others that highlights as a problem “the inability to move patients from the [emergency department] to a ward” and that hospitals should “engage procedures to free inpatient beds well in advance” of access block occurring.2 The capacity of a hospital must have flexibility to deal with demand fluctuations.1 However, we do not agree that the “85% occupancy” figure for optimal efficiency is a candidate for myth status. This threshold is used in various systems around the world. Efficiency is a well recognised concept in queuing theory and depends on setting the utilisation (occupancy) rate at a level where the costs of “underutilised” resources (beds, staff not fully used, etc) are shown to acceptably match the “costs” from delayed care (mortality, morbidity, economic, political, prolonged stay, etc). In particular, quoted occupancy figures often look better than reality because of unopened, unusable beds or data manipulation to improve reported occupancy. The more complex and variable the inputs into a system with multiple competing queues (such as hospitals, where acute admissions may be > 70% of the workload), the greater the need for additional capacity to avoid deferred service. Major acute care hospitals show dramatic daily fluctuations in bed use, with changes between low and high occupancy rates in the order of 15%–20%.3 As inputs and variation increase, the likelihood of marked performance deterioration increases exponentially. Real life (or “clinical modelling”) shows that reported occupancies around or above 85% routinely lead to loss of access to care. No benefits of emergency department or hospital overcrowding have been reported in the medical literature, only harm.4 Relying on developing complex mathematical models before accepting that we are already beyond the acceptable “efficient” occupancy of our current health systems is not a realistic way forward, when patients are dying due to the lack of available appropriate beds.4 Garling, in the overview of his report referred to by Bain and colleagues, states “my recommendations should make more beds available and reduce access block”, but that even with more efficient bed usage “the addition of 350 beds each year” will be required.5 Action is required now and shouldn’t be delayed or subverted by searching for perfect mathematical models. Our hospitals have demonstrably inadequate capacity, resulting in overcrowding with devastating effects. As we have repeatedly stated, it’s all about available beds.

David Mountain · Daniel Fatovich · Sally McCarthy

To the Editor: I agree with the claim by Richardson that “the overlap between [primary care and emergency department (ED)] services is not as important as many have claimed” and that “‘primary care patients’ and ‘ED [Australasian Triage Scale] category 4 and 5’ patients are not interchangeable”.1 A review of the literature — especially from New Zealand — would show there are considerable differences between patients who attend the two types of services. For example, a comparison of patients with asthma attending either a Wellington after-hours medical centre or an ED service located only 800 metres away2 found that the after-hours medical centre was more likely to see younger patients who live further from the service, are given repeat medications, and are referred back to their general practitioner. In contrast, the ED patients were less likely to be referred by a GP and more likely to be admitted to hospital with asthma than patients attending the after-hours centre. Thus, the two services differed in terms of their clinical policies (repeat prescribing and referral) and patients’ demographic characteristics (age, place of residence). I applaud Richardson for highlighting the powerful effects of hospital policies on the behaviour of people outside hospital walls by saying, “it is not the so-called primary care patients who are blocking ambulances from offloading — it is the ‘access block’ patients waiting for beds on the inpatient wards who are inappropriately occupying ED space and staff time”. This claim has nothing to do with the kind of patients who attend primary care services, but more to do with the influence of management policies arising from within hospitals on patient flow from primary care. It confirms research in New Zealand demonstrating how hospital policies (on advertising their services) can have powerful contradictory effects on attendance at EDs. In some cases, people have been subjected to hospitals advertising the clear message that people should attend the ED when they should be seen in primary care instead; and in other cases, people are dissuaded from attending the ED when they are subjected to advertisements about the poor choices people make to attend a hospital. In each case, it is the hospital policy that determines the direction of flow, not the patients in primary care.3-5

Marjan Kljakovic

Cross-border importation of traditional and prescription medications is common, and many of these drugs are not approved by the Australian Therapeutic Goods Administration. Furthermore, counterfeit versions of prescription medications are also available (eg, weight-loss medications, anabolic steroids, and medications to enhance sexual performance). We describe a 54-year-old man with the first Australian case of severe hypoglycaemia induced by imported, laboratory-confirmed counterfeit Cialis. This serves to remind medical practitioners that counterfeit medication may be the cause of severe hypoglycaemia (or other unexplained illness). Clinical recordA 54-year-old male truck driver was admitted to a regional hospital with profuse sweating, slurred speech, ataxia and confusion. He had a history of heavy smoking and moderate alcohol consumption, but denied taking any medications or using recreational drugs. On the evening before his illness, he had four standard alcoholic drinks. On examination, his blood pressure was 150/97 mmHg, body mass index was 33.3 kg/m2, and his score on the Glasgow Coma Scale was 12/15 (eye response, 3; motor response, 6; and verbal response, 3). The rest of the general and systemic examination was unremarkable. In the emergency department, his blood glucose level indicated severe hypoglycaemia (1.1 mmol/L; reference range [RR], 3.0–6.0 mmol/L). After administering 50 mL of an intravenous infusion of 50% dextrose and giving an intramuscular injection of 1 mg glucagon, his Glasgow Coma Scale score improved to 15/15. Subsequently, apart from a high-carbohydrate diet, he required an intravenous infusion of 5% dextrose at a variable rate for 4 days to maintain euglycaemia. His glucose requirement decreased slowly over the following 4 days. He was extensively investigated for hypoglycaemia while in hospital. All other haematological and biochemical parameters, except β-hydroxybutyrate, insulin and C-peptide, were normal. His serum insulin and C-peptide levels, measured on Day 1 and Day 2, were abnormally elevated relative to his low blood glucose level (ie, for the low blood glucose level in this case, the serum insulin level would be expected to be lower). The serum insulin and C-peptide levels had normalised by Day 9 (Box). The serum β-hydroxybutyrate level, measured on Day 2, was particularly low at 0.05 mmol/L (RR, < 0.20 mmol/L), consistent with insulin excess. Magnetic resonance imaging of the pancreas gave negative results for insulinoma. A plasma sulfonylurea screening test, first done on Day 9, gave a negative result. No conclusive diagnosis about this self-limiting hypoglycaemic episode was made during admission. The patient was discharged after making a full recovery. He was advised to self-monitor his capillary blood glucose level and was referred to the endocrinology clinic at our hospital for further evaluation. He attended the endocrinology clinic 2 weeks after discharge. In view of his self-limiting hypoglycaemic episode, specific enquiry was made about the use of oral medication that may have caused the hypoglycaemia. He admitted that, an hour before developing the symptoms, he took a sexual performance-enhancing medication. This was the first time he had taken any medication of this type. The medication had been bought in Vietnam by a friend. This raised the suspicion of contaminated or counterfeit medicine as the cause of the hypoglycaemia. The medication from Vietnam was in a bottle labelled “Cialis 50”. When compared with Cialis manufactured by Eli Lilly, gross differences in packaging, labelling and dose strength were noticed. High-performance liquid chromatography performed by the Australian Therapeutic Goods Administration (TGA) confirmed that one tablet of counterfeit Cialis 50 contained 152.8 mg of glibenclamide and 0.5 mg of sildenafil. The TGA and Eli Lilly Australia were subsequently officially notified. DiscussionThis is the first report of a laboratory-confirmed counterfeit Cialis tablet in Australia. There have been recent warnings about this counterfeit drug and other similar sexual performance-enhancing medications on several health websites.1-4 Cialis (tadalafil), a phosphodiesterase-5 (PDE-5) inhibitor, is a pharmaceutical drug manufactured and marketed by Eli Lilly. It can be obtained only with a prescription, and is dispensed in 5 mg, 10 mg and 20 mg, but not 50 mg, doses. Our case reveals the poor quality-control measures used during the manufacturing process of counterfeit Cialis, which not only contained a lethal dose of a sulfonylurea, but also a subtherapeutic amount of a different agent from the PDE-5 inhibitor class. Glibenclamide is not known to have any sexual performance-enhancing effect, and hypoglycaemia is not a known adverse reaction of tadalafil. Consumption of counterfeit medicines may be harmful. As many countries have not yet enacted deterrent legislation, counterfeiters often do not need to fear prosecution.5 Medicines for erectile dysfunction or sexual enhancement have a huge global market, and this is not the first report of this adverse reaction. An outbreak of hypoglycaemia, secondary to ingestion of sexual performance-enhancing drugs, including counterfeit Cialis and other unlicensed drugs, was reported recently from South-East Asia.6 These drugs also contained high doses of glibenclamide and low doses of sildenafil. The World Health Organization estimates that up to 1% of medicines available in the industrialised countries, and 10% globally, may be counterfeit.7 In Australia, the TGA is an effective regulatory authority; however, despite the regulations, overseas travel and internet purchasing may allow counterfeit medicines to be imported. Under the “Personal import scheme”, many complementary medicines can be legally imported without import permits.8 Additionally, drugs from the PDE-5 inhibitor class, such as tadalafil, which are prescription-only medicines, are not listed under “Prohibited imports and exports (drugs and precursor chemicals)” and so can be purchased on the internet with a prescription from Australia.9 A universal cyberlaw or some other form of international convention is needed to regulate promotion and sales of these types of products on the internet. The WHO acknowledges that increasing international trade in pharmaceuticals, as well as sales via the internet, has further facilitated the entry of counterfeit products into the supply chain. To combat this, in 2006 the WHO helped to create the International Medical Products Anti-Counterfeiting Taskforce (IMPACT).5 Consumers are encouraged to use web sources like the TGA, Health on the Net Foundation, and the WHO to get useful and reliable online health information on medicinal products.10-12 Based on this case, we suggest that health warnings about counterfeit sexual performance-enhancing medications should be published on the TGA website. Glucose, insulin and C-peptide levels during admission Day 1 Day 2 Day 9 Glucose (RR, 3.0–6.0), mmol/L 2.4 2.8 4.7 Insulin (RR, 2–23), mU/L 17 11 0.3 C-peptide (RR, 0.3–1.4), nmol/L 2.6 Not done 0.7 RR = reference range.

Santosh K Chaubey MB BS, MD · Kunwarjit S Sangla MB BS, FRACP · Emershia N Suthaharan MB BS, MD · Yong M Tan MB BS, FRACP, FRCP(Edin)

Putting to rest the myth that emergency department overcrowding is due to a lack of primary care services Australia’s emergency departments (EDs) are dangerously overcrowded, but a study by Buckley and colleagues in this issue of the Journal1 should be the last nail in the coffin of the long-discredited myth that the root cause is a lack of primary care services. This study used a time series approach to identify a real — but clinically insignificant — change in ED workload after the opening of an after-hours primary care service in the New South Wales inland rural city of Wagga Wagga. The Australian public are entitled to receive high-quality and available care in both primary care and emergency settings, but the overlap between these services is not as important as many have claimed.2,3 In a rural location without pre-existing after-hours primary care services, the introduction of such a service, which treated 14 patients daily on average, was associated with an adjusted daily reduction in ED presentations of seven patients with an Australasian Triage Scale (ATS) category of 4 or 5 (lower urgency). As the authors note, because non-admitted low-urgency patients tend to have low resource needs, this reduction of 8% of total ED presentations would correspond to a lesser reduction in workload. Based on published Wagga Wagga Base Hospital data and accepted casemix measures, this reduction would translate to around 3% of this rural ED’s costs and no more than 4% of its ED medical and nursing staff time. These figures are higher than some other Australian estimates,4,5 mostly from studies in cities with pre-existing after-hours services. However, they remain consistent with the observation from these studies that the overall weekly primary care workload in an ED amounts to no more than one patient per hour. In Wagga Wagga, few general practices open for more than 55 hours per week, and the after-hours service opens for 27 hours, but the ED is always open and is the only source of medical care in this community for more than half the 168 hours in each week. It is no surprise that some patients who could reasonably go elsewhere will present to the ED. Buckley et al’s results show that the after-hours clinic treated an average of 3.7 patients per hour. During the hours the clinic was open, the reduction in ED presentations was 1.8 patients per hour and, when it was closed (ie, the rest of the week), the reduction in ED presentations was 0.2 patients per hour. It is unlikely that extending the clinic’s opening hours would make much difference: opening during office hours would probably reduce presentations to existing general practices, and opening later at night would likely be uneconomical. Although, as the study authors note, general practitioners working in EDs in the United Kingdom have been shown to be more cost-efficient than junior medical staff in the same environment, the actual cost of emergency medicine is dominated by infrastructure and staff expenses 24 hours per day.6 EDs have a high average cost per patient and a low marginal (incremental) cost for additional low-acuity presentations, especially compared with off-site after-hours clinics, where expenses are dominated by medical labour, and the average and marginal costs are much closer together. Even if patients were 100% interchangeable, a new after-hours service would likely represent an increase in total cost to the community, because it would not reduce the need for the “public good” of a 24-hour service available at the hospital. Despite its limitations, this study confirms that “primary care patients” and “ED ATS category 4 and 5 patients” are not interchangeable. It is to be expected that there is some overlap between patients who might want to present to an ED and those who might want to go to a GP — just as there may be overlap between patients going to a GP or a gynaecologist for a Pap smear, or between those going to a thoracic surgeon or a respiratory physician for investigation of a lung mass. However, the finding that 96% of the weekly workload of an ED cannot be substituted by an after-hours service confirms that patients are largely presenting appropriately. By comparison, at least a third of average ED staff workload (and more than half in some places) consists of providing care to those who have completed their emergency treatment and are waiting for an inpatient bed,7 sometimes for days. Australian EDs are dangerously overcrowded with patients, many of whom should not be in EDs because they would be better managed elsewhere. But it is not the so-called primary care patients who are blocking ambulances from offloading8 — it is the “access block” patients waiting for beds on the inpatient wards who are inappropriately occupying ED space and staff time.

Drew B Richardson MB BS(Hons), FACEM, GradCertHE

Objective: To assess the impact of the opening of an after-hours general practice clinic on the number of daily low-urgency presentations to the nearby emergency department.Design, participants and setting: Retrospective time series analysis of emergency presentation data, from the New South Wales Health Emergency Department Information System, for all patients presenting to the emergency department of Wagga Wagga Base Hospital between January 1998 and October 2008.Main outcome measures: Daily emergency department presentations, before and after the March 2003 opening of the after-hours clinic, of patients triaged as Australasian Triage Scale (ATS) category 4 or 5 (at any time of day, and during the hours of operation of the clinic), and of patients triaged as ATS category 1, 2 or 3 (at any time of day).Results: After adjusting for long-term trends and weekly and annual cycles, the opening of the after-hours clinic was associated with a daily reduction of 7.04 patients (95% CI, 5.39–8.70) in emergency department presentations with an ATS category of 4 or 5. This represented an 8.2% reduction in total presentations (95% CI, 6.2%–10.2%). Presentations of ATS category 1, 2 or 3 patients rose by 1.36 patients a day (95% CI, 0.36–2.35), representing 1.6% of total presentations (95% CI, 0.4%–2.7%). The impact of the after-hours clinic was best modelled by a gradual permanent change.Conclusion: An after-hours general practice clinic was associated with a reduction in low-urgency presentations to the emergency department in Wagga Wagga.

David J Buckley BVSc(Hons), MVSc · Paul W Curtis MB BS, MHA, FRACMA · Joseph G McGirr MB BS, BSc(Med), FACEM

To the Editor: We read with interest Walters and Dawson’s call for a clinical revolution to tackle access block1 and are heartened by the interest shown by general physicians in a problem that primarily affects the emergency department (ED). The efficient management of admitted medical patients is paramount to patient flow within the hospital, and “buy-in” from general physicians is essential. When considering any new model of care, it is important to note that longer patient assessments in ED by emergency doctors has a relatively small effect on access block; the claim that the length of assessments is a significant factor in access block has been established as a “myth” by investigators who have mapped process times.2 Therefore, it is unlikely that substituting one workforce of acute physicians for another would make any difference to overall patient flow through the ED. On the contrary, it is likely to be associated with increased costs3 and adverse effects on the emergency medicine labour supply.4 In addition, the ability and willingness of the general physician workforce to implement and sustain the newer role of “acute physician” is unknown. The root cause of access block lies in ward-bed shortages, ward processes and community capacity, which should be solved by improved flow processes across the continuum of care. Access block will not be solved by a second tier of acute physicians duplicating the role of emergency physicians. However, there are many aspects of Walters and Dawson’s model of change that would improve patient flow, in particular: improved rostering of medical staff; improved access to pathology and radiology services; and, perhaps, specific retraining of medical staff in the efficient discharge of inpatients. These aspects should be rigorously explored as we strive together to tackle access block.

Biswadev Mitra · Peter A Cameron · Pieter De Villiers Smit

To the Editor: Walters and Dawson1 correctly highlight access block (hospital overcrowding) as a whole-of-system problem. Acute medical assessment and admission units (AMAAUs), or other similar incarnations in Australia and New Zealand, are part of the solution, although the evidence presented is low-level non-Australasian data. The reduced length of stay achieved by these units and reported in papers cited by Walters and Dawson would, if replicated in Australasia, produce additional capacity, improving bed availability and patient flow. As has been repeatedly stated: it’s all about available beds!2 However, Walters and Dawson’s article stretches well beyond the evidence in its approach to emergency department (ED) roles and the interactions between AMAAUs and EDs. None of the cited studies suggested that AMAAUs provide better environments than EDs for sick undifferentiated patients. None studied effects that AMAAUs have on ED treatment and none proposed interventions specifically designed to alter ED management. They essentially examined improved patient journeys for front-loaded AMAAU versus standard (slower) general medical inpatient care. In addition, Walters and Dawson imply that these changes related to introduction of the United Kingdom’s 4-hour rule. However, many references were either non-UK or not specific to the 4-hour rule. Rigorous research in an Australasian context would be required before adopting models from a different system. The authors promote a view that undifferentiated acutely sick patients bypass the ED to be managed by “new” acute-care specialists. No evidence is presented to support this change, and it is difficult to see how this would be a sensible policy for Australia and NZ, which have mature ED systems. Emergency physicians are specialists specifically trained and skilled in early diagnosis, management and disposition of the undifferentiated, unwell patient. What is required is a system that builds on the excellent start made by the ED, removes the blocks to patient care caused by waiting for beds in the ED and then continues to emphasise rapid diagnosis, early management, disposition and flow. This is what AMAAUs can deliver and why they should be effective. Australasian EDs already provide an exemplary service in a difficult, access-blocked environment. What patients need is sufficient hospital capacity — hospitals that provide enough appropriate beds. We look forward to seeing AMAAU staff meet this need in partnership with their emergency physician colleagues. In summary, it’s all about available beds, about having enough overall capacity and optimising patient flow to maximise bed availability.2 The only revolution required is for governments to recognise this fundamental precept.

David Mountain · Daniel M Fatovich · Drew B Richardson · Sally M McCarthy

To the Editor: Although written from a United Kingdom perspective, the recent article by Walters and Dawson1 suggests a change in the clinical culture within hospitals, so that patient care and throughput can be improved. A critical factor in achieving change is the creation of an acute medical assessment and admission unit (AMAAU) within each district hospital. Characteristics of the AMAAU will “depend on local circumstances”: there is no one size that fits all.1 Because of Australia’s unique demography, and the number of communities beyond the reach of tertiary centres, many primary-care physicians (general practitioners and “rural generalists”) provide the continuum of care required by patients, both within the community and within their local hospitals (the acute admission, ongoing inpatient care and discharge planning). Twenty-first-century GPs deal daily with patients needing management of multiple comorbidities and the consequences of polypharmacy (the “sick general” and “complex elderly” clinical streams1). GP training prepares doctors for these responsibilities and could easily be expanded to include an AMAAU role for interested GPs, especially those in outer urban and major rural areas. The advent of AMAAUs is an opportunity to change the mindset in medicine: after 8 to 9 years of primarily hospital-based training, some GPs suddenly have no hospital access! This would seem to be a callous waste of talent and resources.

Frank R Jones

To the Editor: Walters and Dawson1 highlight growing interest in new models of care aimed at ameliorating hospital-bed pressures and access block. They advocate acute medical assessment and admission units (AMAAUs) as a potential solution, and claim, principally based on the United Kingdom’s experience, that these units can significantly improve clinical care and patient outcomes. A recent systematic review confirms that these units (which have attracted several different synonyms) have promise, although controlled trials have yet to be performed, and publication bias remains a potential confounder.2 Experience with such units in Australia and New Zealand is growing, with more than 30 units in operation, and up to another 15 due to open over the next few years. Several national workshops conducted during the past 12 months have allowed staff of the units to share lessons and insights, and to debate how to balance service needs with resource availability. Operating standards for AMAAUs have been developed by the Internal Medicine Society of Australia and New Zealand (IMSANZ),3 which represents consultant general physicians. A recent survey shows the operations of Australasian units concord, in the most part, with these standards.4 We caution against Walters and Dawson’s suggested separation of AMAAU physicians into two streams — acute physicians working shifts, and ward-based general physicians responsible for patients requiring transfer from the AMAAU. Given that at least half of AMAAU patients will require transfer to inpatient wards, and many may warrant ongoing outpatient care even if discharged from the AMAAU, the need for continuity of care is paramount at the interface between the AMAAU and ward or clinic. To minimise the number of handovers and their attendant hazards and inefficiency, the medical team assessing and managing the patient in the AMAAU should ideally be the same team that provides ongoing inpatient (and indeed subsequent outpatient) care. This practice also eliminates any confusion around who is ultimately responsible for decisions about individual patient care, particularly for patients who remain in the AMAAU for any length of time. General physicians can acquire and maintain skills in acute medicine by making use of professional development programs sponsored by the IMSANZ. Clinical directors are needed in AMAAUs to oversee unit operations, develop policies and procedures, and provide capacity for rapid consultant response if on-call consultants are temporarily unavailable. The real challenge, to which Walters and Dawson refer, is the need for health care professionals to recognise that whole-of-hospital redesign solutions — which include AMAAUs — are needed, if access block in emergency departments is to be successfully overcome.

Ian A Scott · John W Henley

To the Editor: The Journal took a significant step forward in publishing the three articles on access block in the 6 April 2009 issue.1-4 Walters and Dawson’s viewpoint article,4 in a later issue, touches on some ideas that will be useful in finding solutions to access block — ideas that some hospitals are implementing. However, I am not sure a microsolution aimed purely at acute medical patients can be called a whole-of-hospital revolution. The acute medical assessment and admission unit (AMAAU) is potentially a good idea. Fortunately, many hospitals all over Australia already have units that are highly efficient at the role that is proposed for it — they are called emergency departments (EDs). Most acute medical patients can be identified as needing admission after a few seconds in the ED by experienced emergency physicians. The remaining patients need some basic pathology or imaging service before a decision can be made, which should take an hour at the most. Having secondary inpatient units providing this role to the community via direct general practitioner referrals, as well as having some patients bypassing the ED by being cherry-picked by inpatient teams, may generate inefficient duplications of service. The AMAAU has merit, streaming patients to the right specialty and the right inpatient bed early in their presentation. Emergency physicians have largely known this for over a decade and these kinds of units have already been introduced in hospitals all over the country. Nepean Hospital, in western Sydney, has the PECC (Psychiatric Emergency Care Centre), AGS (Acute Gynaecological Service), MAU (Medical Assessment Unit), EDMAU (ED Medical Assessment Unit), EMU (Emergency Medical Unit) and ASU (Acute Surgical Unit), to name just a few acronyms. Unfortunately, this does not deal with the 20 patients in the ED, already admitted and sorted, waiting for an inpatient bed at 8 am on a Monday. Increased inpatient bed numbers to cope with the predicted acute ED admissions and the planned elective surgical workload must be the number-one priority. Once we have bed numbers to cope with demand, then we can plan how to use them. I propose my own revolution. We need to provide a true 7-day-a-week service to our hospital inpatients. Ward rounds should be conducted 7 days a week. All inpatient consults, including those of allied health practitioners, should be completed on the same day, including weekends. All complex imaging should be completed on the day it is ordered, not the next working day, with formal reports available the same day. Once we acknowledge that acute hospital medicine does not fit in with the 38-hour working week, then we can truly start acting as patient advocates.

James L Mallows

More sensitive assays may provide more information, but we are not yet sure of the clinical relevance of this information The introduction of troponin measurement into clinical practice in Australia 10 years ago led rapidly to its widespread use as the marker of choice for diagnosis and risk stratification of patients with acute coronary syndrome (ACS). However, opportunities remain for improving risk assessment in “troponin-negative” patients, many of whom will have adverse events. This has led to the development of new, improved assays that are able to measure down to much lower concentrations than before (10–100-fold lower than current assays), and that increase the detection of acute myocardial infarction, as shown in two recent cohort studies.1,2 The improved analytical performance of these assays may be particularly useful in the early period following the onset of chest pain. These two studies indicated improved diagnostic accuracy of samples taken from patients with chest pain, both at the time of presentation to the emergency department (ED), and within 3 hours of symptom onset.1,2 This improved early sensitivity may lead to significant benefits in ruling out ACS, and in risk assessment, diagnosis and management of patients with ACS, although neither of these studies provided corroboration with clinical outcome. The development of these new “highly sensitive” assays for cardiac troponin raises many questions about their clinical application, including the degree of analytical precision, the medicolegal definition of myocardial infarction, earlier detection and improved management of patients with ACS, as well as the interpretation of elevated cardiac troponin levels in other clinical situations. The current accepted international definition of myocardial infarction — the “universal definition of myocardial infarction”3 — requires a rise or fall in the level of cardiac biomarkers (preferably troponin) with at least one value above 99th percentile of the upper reference limit, along with at least one clinical indicator (symptoms of ischaemia, new ischaemic changes or new Q waves on electrocardiogram, new imaging evidence of loss of viable myocardium or a new regional wall motion abnormality). The use of assays that do not have optimal precision (coeffficient of variation [CV] < 10% at the decision level) is not recommended, although, a variety of the older, less precise assays are still in clinical use. New, highly sensitive (hs) assays have the recommended degree of analytical precision, and the first (Roche hsTnT, Roche Diagnostics) has been launched while others are in preparation. Their use would lead to an increase in the diagnosis of myocardial infarction. Measuring low levels of troponin introduces an additional confounder — that of significant biological variability4 — which would require an increase in the traditionally accepted 20% serial change of troponin level over baseline values that is required to meet the definition of myocardial infarction.5 The application of cardiac troponin measurement in risk stratification of patients presenting with ACS has been strongly supported by clinical data. Measurable cardiac troponin levels in these patients, even concentrations below that corresponding to the recommended assay precision (CV < 10%), are associated with adverse clinical outcomes. In addition, aggressive management has been shown to improve clinical outcome in these high-risk patients. It is possible that the hs assays will improve the identification of high-risk patients who benefit from aggressive management, but this will require clinical validation. From an ED perspective, the new assays present the possibility of identifying patients at very low risk of 7-day or 30-day adverse events at a much earlier stage. Two hs troponin assays at least 3 hours apart, or one assay taken at least 6 hours after symptom onset may be accurate in ruling out myocardial infarction in the ED, but the evidence for this approach is so far limited.2 This should allow for more immediate decision making in relation to proceeding to further testing (such as an exercise stress test or stress echocardiography) and discharge from the ED, and could significantly decrease overnight admissions of patients with possible cardiac chest pain. The use of any biomarker assay in managing chest pain or possible ACS should always be done in conjunction with a full clinical assessment to ensure appropriate risk stratification. The other common clinical question is how to interpret cardiac troponin levels in patients without clinical features of ACS. There have been several reports suggesting that normal healthy people without cardiac disease may have very low, but detectable levels of troponin present at all times.6,7 This raises the intriguing possibility of cardiomyocyte turnover and renewal.8 Low levels of cardiac troponin have also been identified, and have been shown to be correlated with structural heart disease, diabetes mellitus and chronic kidney disease in a small percentage of the general population.9 Screening of asymptomatic elderly men for serum troponin predicted the risk of future cardiac events.10 Although troponin release has traditionally been thought to be caused by cardiomyocyte necrosis, recent information suggests that troponin may be released after ischaemia without necrosis in patients undergoing stress testing.11 A 10-fold increase in low-level troponin concentration has also been identified in athletes after marathon running.7 Elevated troponin levels are not uncommon in patients in intensive care units, and possible causes include supply/demand ischaemia and alterations in myocyte membrane permeability or leakage. The likelihood of ACS in these patients is low in the absence of usual symptoms or evidence of acute ischaemia or infarction. Cardiac troponin levels may also be elevated by non-coronary causes including myocarditis, aortic dissection, Tako-tsubo syndrome, pulmonary embolism, cardiac trauma, sepsis, tachycardia, severe heart failure, and “false positives” that include heterophile antibodies and analytical imprecision. All elevations in cardiac troponin concentrations, and particularly in low-level measurements, should be interpreted in the context of the pretest probability of ACS, as well as possible non-coronary causes of troponin release. In conclusion, our understanding and interpretation of troponin concentration and use of the new highly sensitive assays continue to evolve. This may offer us greatly enhanced opportunities for early diagnosis, risk assessment and improved management, but their widespread use will require clinical validation. More than ever before, however, there is a clinical imperative not to immediately equate detectable troponin concentration with ACS, but to interpret each result in its clinical context.

Con N Aroney MD, FRACP, FCSANZ · Peter E Hickman MB BS, PhD, FRCPA · Hans G Schneider MD, FRACP, FRCPA · Jillian R Tate BSc(Hons), MSc · Martin Than FACEM, FCEM

Hospital funding based on achieving targets for numerical key performance indicators was implicated in Queensland’s Bundaberg Base Hospital scandal and has driven hospital data fraud in Victoria and New South Wales. Nationally uniform legislation is required to make health service reporting standards consistent and to criminalise public sector data fraud. Urgent action is needed to develop realistic outcome measures that base hospital funding more on the quality and safety of patient care and less on patient throughput numbers.

Antony Nocera FACEM, MSc(Emergency Planning and Disaster)